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Biomedical subjects

U van Laak

Publications and source records attributed to U van Laak.

7 recordsLinked to original sources
PubMed1999

[Severe decompression sickness in divers].

The term "decompression illness (DCI)" is a disorder which arises from the presence of ectopic gas bubbles following decompression. Scuba diving poses the risk of two typically clinical syndromes: decompression sickness (DCS) and arterial gas embolism (AGE). DCS results from the formation of gas bubbles in the tissues of the body and in the blood due to rapid reduction of the environmental pressure. AGE is caused by pulmonary overinflation if the breathing gas cannot be exhaled adequately during the ascent. Although the pathophysiological mechanisms of these two disorders are quite different, both of them lead to the same result: inert gas bubbles that may cause impairment of vital functions due to hypoxia. Recognizing the signs and symptoms of DCI is the first step of the therapy. The emergency treatment contains: basic life support, advanced life support--if necessary, horizontal positioning of the victim, administration of 100% normobaric oxygen via face mask or endotracheal tube, rehydration, rapid transportation to the nearest emergency department/hyperbaric facility for definitive treatment in order to prevent serious neurological sequelae.

Barotrauma↗
PubMed1994

[Successful treatment with hyperbaric oxygen following severe cerebro-arterial gas embolism].

We report on a patient suffering from a severe cerebral arterial gas embolism associated with decompression from a simulated high pressure chamber dive. Treatment with hyperbaric oxygen (HBO) commenced immediately after the accident and was continued subsequently for 8 weeks with a total of 49 HBO-sessions. Despite initial transitory amaurosis and flaccid tetraplegia lasting for two weeks the patient made a near complete recovery except for circumscript numbness and paraesthesia confined to the left tibia and palm. This case underscores the need to consider patients with cerebral arterial gas embolism for HBO treatment and the potential value of a subsequent long-term HBO therapy.

Adult↗
PubMed1994

Exercise effects on central venous nitrogen tensions after simulated non-decompression dives.

In five subjects we examined the effect of exercise on the pattern of central venous (right atrial) N2 tensions (PVN2) after ascent from simulated non-decompression dives. The dives consisted of exposure to air at 3 bar for 20 min with 10 min of exercise (workload 75 W) at depth to achieve near-complete N2 saturation of the muscles. After the dive the subjects rested or, on another day, exercised for 30 min (workload 100 W) starting 10 min after completing the ascent. Blood samples taken every 10 min until the 60th min and 90 min after the dive were analyzed for PVN2 using a manometric Van Slyke apparatus. The amount of N2 eliminated was estimated from the PVN2 by adapting the Fick principle. Immediately after the ascent, PVN2 were 950 +/- 39 and 942 +/- 27 mmHg, respectively, in the rest and experiment series. In the rest experiments PVN2 continuously decreased to 606 +/- 8 mmHg 90 min after the dive, remaining significantly higher (P < 0.05) than before the dive. Exercise caused the PVN2 to increase beyond the corresponding levels of the rest experiments (P < 0.05 at 20 and 30 min exercise). After the exercise PVN2 rapidly declined, reaching predive levels 60 min after the ascent. Exercise increased N2 elimination to 970 +/- 143 ml, whereas it had been 311 +/- 61 ml (P < 0.05) in the corresponding phase of the rest experiments. We conclude that if extensive supersaturation and bubble formation can be avoided, such as probably was the case in our shallow non-decompression dives, exercise after the ascent accelerates N2 elimination.

Adult↗
PubMed1993

[Clinical aspects, pathophysiology and therapy of decompression sickness].

The primary treatment of decompression illnesses (arterial gas embolism and all types of decompression sickness) is recompression therapy, combined with hyperbaric oxygen breathing. It is essential to initiate treatment as soon as the symptoms arise. However, prior to hyperbaric oxygen therapy--particularly with any delay in starting recompression--specific supportive therapy for severe decompression-related injuries is mandatory after first-aid treatment has been given. The preferred supportive treatment would be 100% normobaric oxygen breathing, oral or better i.v. fluids (crystalloids or dextrose saline), flat position on the back, and organization of appropriate means of transportation to the nearest hyperbaric center. Large doses of corticosteroids as well as anticoagulants are under discussion, but there is some evidence that steroids and medium doses of acetylsalicylic acid, given initially, may be of certain benefit for patients suffering from cerebral- and spinal-cord trauma due to decompression accidents. There is evidence that latency of onset of decompression illnesses is a prognostic indicator. Nevertheless, urgent HBO therapy in a hyperbaric chamber suitable for intensive care under pressure is mandatory for all severe decompression disorders.

Decompression Sickness↗